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Aim: The tumor microenvironment in pancreatic cancer, characterized by abundant desmoplastic stroma, has been implicated in the failure of chemotherapy. Therefore, developing therapeutic strategies targeting tumor and stromal cells is essential. Triptolide, a natural compound derived from the plant Tripterygium wilfordii, has shown antitumor activity in various cancers, including pancreatic cancer.

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Therapeutic Potential of Carbon Dots Derived from Phytochemicals as Nanozymes Exhibiting Superoxide Dismutase Activity for Anemia.

ACS Appl Mater Interfaces

January 2025

State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.

Anemia is a potentially life-threatening blood disorder caused by an insufficient erythroblast volume in the circulatory system. Self-renewal failure of erythroblast progenitors is one of the key pathological factors leading to erythroblast deficiency. However, there are currently no effective drugs that selectively target this process.

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Multifunctional CuBiS-BP@PEI Radiosensitizer with Enhanced Reactive Oxygen Species Activity for Multimodal Synergistic Therapy.

ACS Biomater Sci Eng

January 2025

Fujian Provincial Key Laboratory of Advanced Materials Oriented Chemical Engineering, Fujian-Taiwan Science and Technology Cooperation Base of Biomedical Materials and Tissue Engineering, Engineering Research Center of Industrial Biocatalysis, College of Chemistry and Materials Science, Fujian Normal University, Fuzhou 350007, China.

Development of radiosensitizers with high-energy deposition efficiency, electron transfer, and oxidative stress amplification will help to improve the efficiency of radiotherapy. To overcome the drawbacks of radiotherapy alone, it is also crucial to design a multifunctional radiosensitizer that simultaneously realizes multimodal treatment and tumor microenvironment modulation. Herein, a multifunctional radiosensitizer based on the CuBiS-BP@PEI nanoheterostructure (NHS) for multimodal cancer treatment is designed.

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IP6K1 rewires LKB1 signaling to mediate hyperglycemic endothelial senescence.

Diabetes

January 2025

Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.

Diabetes is a major risk factor for cardiovascular disease, but the molecular mechanisms underlying diabetic vasculopathy have been elusive. Here we report that inositol hexakisphosphate kinase 1 (IP6K1) mediates hyperglycemia-induced endothelial senescence by rewiring the liver kinase B1 (LKB1) signaling from activating the adenosine monophosphate-activated protein kinase (AMPK) pathway to the p53 pathway. We found that hyperglycemia upregulated IP6K1, which disrupts the Hsp/Hsc70 and carboxyl terminus of Hsc70-interacting protein (CHIP)-mediated LKB1 degradation, leading to increased expression levels of LKB1.

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Background: Epstein-Barr virus (EBV) is implicated as a necessary factor in the development of multiple sclerosis (MS) and may also be a driver of disease activity. Although it is not clear whether ongoing viral replication is the driver for MS pathology, MS researchers have considered the prospect of using drugs with potential efficacy against EBV in the treatment of MS. We have undertaken scientific and lived experience expert panel reviews to shortlist existing licensed therapies that could be used in later-stage clinical trials in MS.

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